Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 13-year-old boy who was known to have Fanconi's anemia for five years. For treatment of this condition he was given androgens and corticosteroids. Two months before his death, severe varicella developed complicated by pneumonia, jaundice, and prolonged fever; all of which resolved during a five-week hospitalization. Three weeks later he died of Clostridium septicum sepsis caused by necrotizing enterocolitis. At autopsy he was found to have multiple hepatocellular neoplasms. A striking feature of the neoplasms was cholestasis. The liver also showed peliosis hepatis. The association of the use of certain androgenic steroids with hepatic neoplasms histologically resembling hepatocarcinomas, but characterized by lack of metastases and apparent reversibility, suggests the desirability of a new nomenclature for these hepatocellular lesions.
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PMID:Multiple hepatic tumors and peliosis hepatis in Fanconi's anemia treated with androgens. 19 56

An important adaptation of the gastrointestinal tract to the extrauterine environment is its development of a mucosal barrier against the penetration of harmful substances (bacteria, toxins and antigens) present within the intestinal lumen. At birth, the newborn infant must be prepared to deal with bacterial colonization of the gut, with formation of toxic byproducts of bacteria and viruses (enterotoxins and endotoxins) and with the ingestion of antigens (milk proteins). These potentially noxious substances if allowed to penetrate the mucosal epithelial barrier under pathological conditions can cause inflammatory and allergic reactions which may result in gastrointestinal and systemic disease states. To combat the potential danger of invasion across the mucosal barrier the infant must develop an elaborate system of defence mechanisms within the lumen and on the luminal mucosal surface which act to control and maintain the epithelium as an impermeable barrier to uptake of macromolecular antigens. These defences include a unique immunological system adapted to function in the complicated milieu of the intestine as well as other non-immunological processes such as a gastric barrier, intestinal surface secretions, peristaltic movement and natural antibacterial substances (lysozyme, bile salts) which also help to provide maximum protection for the intestinal surface. Unfortunately, during the immediate postpartum period, particularly for premature and small-for-dates infants, this elaborate local defence system is incompletely developed. As a result of the delay in the maturation of the mucosal barrier newborn infants are particularly vulnerable to pathological penetration by harmful intraluminal substances. The consequences of altered defence are susceptibility to infection and the potential for hypersensitivity reactions and for formation of immune complexes. With these reactions comes the potential for developing life-threatening diseases such as necrotizing enterocolitis, sepsis and hepatitis. Fortunately, 'nature' has provided a means for passively protecting the 'vulnerable' newborn against dangers of a deficient intestinal defence system, namely human milk. It is now increasingly apparent that human milk contains not only antibodies and viable leucocytes but many other substances which can interfere with bacterial colonization and prevent antigen penetration.
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PMID:Gastrointestinal host defence: importance of gut closure in control of macromolecular transport. 26 21

Necrotizing enterocolitis--a highly letal disease in the newborn period--is diagnosed in about 1--2% of the admissions to a nursery. The marcroscopic lesions are basically necroses predominantly found in the ileum, colon and jejunum. Untreated they lead to perforation, peritonitis and sepsis. The predisposing factors include such as perinatal complications, immaturity and umbilical vein catheterization; the main symptoms are bile stained vomiting and blood-streaked diarrhea, followed by signs of fulminant sepsis and peritonitis. The most typical roentgenographic findings are intramural air (pneumatosis intestinalis) and in more advanced cases pneumoperitoneum (free peritoneal air) and portal vein gas. The current plan of management--consisting of immediate withdrawal of oral feeds, gastric suction, intravenous fluid therapy, treatment of shock and administration of antibiotics--and the indication for operation are discussed. Perinatal stress and secondary bacterial invasion of the intestinal lesions seem to play an important role in the etiology of the disease. An early nutrition of the healthy immature with human breast milk seems to reduce the incidence of necrotizing enterocolitis or at least has a mitigating influence on the later course of the disease. The mortality in our own series--as reported--was high (6 patients: 1 survivor, mortality: 83%) as 4 of the patients were admitted with gross symptoms of intestinal perforation and severely shocked.
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PMID:[Necrotizing enterocolitis (pediatric review)]. 33 53

Necrotizing enterocolitis has become the most common condition requiring emergency surgical treatment in the newborn infant, far surpassing all major congenital anomalies in number of presentations and in deaths after surgical treatment. No single cause for the disease is known. Necrotizing enterocolitis is characterized by ischemic necrosis of the intestine, with minimal inflammation. In 25 of 50 per cent of patients, surgical resection of gangrenous bowel is necessary. Operation is reserved for infants with intestinal perforation or grangrene. Recent refinements of indications for operation often permit surgical intervention to coincide with the advent of intestinal gangrene. At operation, expeditious resection of frankly necrotic bowel and exteriorization of the marginally viable ends is all that should be attempted. Special problems postoperatively consist of management of sepsis, maintenance of nutrition and vigilant observation for early and late complications, particularly the development of ischemic intestinal stricture.
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PMID:Necrotizing enterocolitis in the neonate. 36 4

A premature infant with acute necrotizing enterocolitis, Escherichia coli sepsis, and disseminated intravascular coagulation developed spontaneous bilateral hyphemas at 3 days of age. The necrotizing enterocolitis was associated with gas bubbles in the intestinal walls. The anterior chambers of both eyes also contained bubbles of gas, formed possibly by a mechanism similar to those in the intestine.
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PMID:Pneumatosis oculi and spontaneous hyphema in association with pneumatosis intestinalis. 38 51

Necrotizing enterocolitis (NEC) is usually described as occurring in newborn premature of low-birth-weight infants who have been stressed by hypoxia, exchange transfusion, or severe sepsis. It occasionally occurs in full term neonates. The age of onset is between day 1 and day 35. This communication describes the occurrence and course of NEC in a 3 mo old infant with a short intestine.
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PMID:Necrotizing enterocolitis occurring in an infant three months of age. 89 62

Twenty-seven ill neonates with enterovirus infections were studied to learn if enterovirus infection can be distinguished from neonatal sepsis. Enterovirus infection was associated with the summer-fall season (93%), recent maternal illness (59%), absence of other perinatal problems (81%), and findings of fever (93%), viral meningitis (62%), diarrhea (81%), and rash (41%). Four children developed thrombocytopenia and three necrotizing enterocolitis. Three children died, all with Coxsackie B virus infections that likely were acquired in utero. Although no single feature is pathognomonic, this constellation of epidemiologic and clinical findings, coupled with negative bacterial cultures, should suggest the possibility of neonatal enterovirus infection.
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PMID:Enterovirus infections in neonates. 97 29

Emphysematous gastritis associated with gram-negative sepsis is described in a leukemic child on chemotherapy and steroids. Bubbly-appearing air and thickening of the gastric wall were radiographically demonstrated. This is analogous to the demonstration of air within the thickened bowel wall in necrotizing enterocolitis, which is not unusual in seriously ill leukemic children. Gastric involvement has not been previously reported.
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PMID:Emphysematous gastritis in a leukemic child. 106 99

Natural surfactant (Surfactant TA, Survanta, CLSE, SF-RI 1, Curosurf and human surfactant obtained from amniotic fluid) therapy for RDS in very premature infants has been evaluated in 17 controlled clinical trials. Uniformly intratracheal surfactant administration caused a decreased intensity of mechanical ventilation during the first hours (reduced inspiratory pressure, reduced oxygen requirements) as an immediate effect of surfactant administration. Metanalysis reveals barotraumatic pulmonary complications mainly, pneumothorax and pulmonary interstitial emphysema to occur less frequently in surfactant-treated infants in virtually all trials; an increased incidence of survival without bronchopulmonary dysplasia following surfactant treatment was observed in 10 controlled clinical trials. The incidence of other complications of prematurity (intracranial hemorrhage, patent ductus arteriosus and necrotizing enterocolitis) was unchanged following natural surfactant treatment. Dosing of natural surfactant is still under investigation, however recent data indicate that the initial dose should not be less than 100 mg/kg b.w. and retreatment should be given to infants with unsatisfactory response (i.e. fraction of inspired oxygen (FiO2) > 40%). Timing of surfactant treatment still remains controversial. Prophylactic treatment shortly following birth has been compared with rescue-treatment, i.e. surfactant administration to infants suffering from manifest RDS in most studies 4-8 h after birth. Conflicting data from 5 controlled trials may be interpreted as follows: prophylactic treatment seems to be favourable for extremely premature infants (GA < or = 26 weeks) and rescue treatment seems to be adequate for infants of 27-30 weeks of gestation. Intratracheal surfactant instillation in very premature infants did not result in an improved lung function for 24 h to 48 h in all patients. Ten--25% of study infants were reported to be "non-responders", i.e. infants without sustained decrease in oxygen requirements (i.e. FiO2 > 40%). Various factors may be operative including congenital bacterial infections (sepsis or pneumonia), lung hypoplasia and cardiac failure. Inactivation of surface properties of natural surfactant caused by a leakage of proteins across the alveolar-capillary membrane was observed in experimental and clinical studies. Current investigations focus on a combination of postnatal steroids and surfactant treatment to improve lung function and outcome in "non-responders". As long as any controlled clinical studies are being published, this approach remains experimental. Up to now, any controlled clinical trials have been performed to assess different modes of artificial ventilation (e.g. high frequency oscillating ventilation versus conventional ventilation) combined with surfactant therapy. Data obtained from premature animals given natural surfactant indicate any advantage with respect to gas exchange and lung histology to result from high frequency ventilation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural surfactant for neonatal respiratory distress syndrome in very premature infants: a 1992 update. 129 66

We reviewed jaundiced infants born between 1971 and 1989. Jaundice was diagnosed in infants whose serum bilirubin level was found to be 154 umol/l or greater. Of 88,137 livebirths, 10,944 (12.4%) were jaundiced. The most common aetiological factor was prematurity (20.3%), followed by ABO erythroblastosis (5.5%), sepsis (1.8%), Rh erythroblastosis (1.8%), bruising (1.3%), multifactorial (1.0%) and glucose-6-phosphate dehydrogenase deficiency (0.5%). In the remainder (67.8%) no cause was found or inadequate investigations were performed to determine a cause. During the period under review there was a significant increase (r = 0.91) in the proportion of newborn infants with jaundice of prematurity, in those not investigated (r = 0.92) and a decrease in the proportion with bruising (r = -0.90) as the cause. Phototherapy was used on 4,126 (37.7%) infants and exchange transfusion performed on 248 (2.3%). Causes of jaundice in infants requiring exchange transfusion were Rh erythroblastosis (108, 43.6%), ABO erythroblastosis (58, 23.4%), jaundice of prematurity (44, 17.7%) and a variety of causes in the remaining 38 (15.3%). Death occurred in 164 (1.5%) infants. In only 7 (4.3%), however, was the death possibly related to hyperbilirubinaemia or its treatment (Rh erythroblastosis (4), necrotizing enterocolitis following exchange transfusion (2) and pulmonary haemorrhage following exchange transfusion (1)). Phototherapy proved safe with no deaths attributable to its use.
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PMID:Jaundice: clinical practice in 88,000 liveborn infants. 144 22


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